Expression of Class I and Class II major histocompatibility complex antigens on epithelial cells in recurrent aphthous stomatitis

Abstract

The concept of an immunopathogenesis in the establishment and progression of the recurrent aphthous stomatitis (RAS) lesion is well accepted. In this study the expression of Class I and Class II major histocompatibility complex (MHC) antigens on the epithelial cells in the preulcerative, ulcerative and healing phases of RAS lesions was investigated using monoclonal antibodies in an immunohistological technique. Both Class I and Class II MHC antigens were found on the basal cells in preulcerative lesions. As the lesions progressed to the ulcerative phase, antigen expression occurred on the cell membranes throughout the entire thickness of the epithelium. With healing, the expression of both Class I and Class II MHC antigens on epithelial cells declined to a stage where there was little or no detectable antigen on the cell membranes. Although cytotoxity of epithelial cells in RAS lesions is accepted the role of MHC antigen expression on these cells is uncertain and remains to be ascertained. Nevertheless, the results of the present study indicate that MHC antigens are expressed by epithelial cells in RAS and their expression follows a defined sequence.

IL-1B and IL-6 gene polymorphisms encode significant risk for the development of recurrent aphthous stomatitis (RAS)

“…4 The majority are CD45RO + memory cells. 4 Adjacent keratinocytes become HLA-DR 5 and ICAM-1 positive and local blood vessels express Eselectin and VCAM-1. 6 These changes are consistent with release of pro-inflammatory cytokines such as IL-1, IL-6, TNF and interferon-␥.…”

Raised anti-endothelial cell autoantibodies (AECA), but not anti-neutrophil cytoplasmic autoantibodies (ANCA), in recurrent oral ulceration: modulation of AECA binding by tumour necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ)

“…The finding that target antigens are down-regulated by IFN-is intriguing and significant, as the expression of keratinocyte CD54 (intercellular adhesion molecule-1 (ICAM-1)) [44] and HLA-DR [45,46] in ROU lesions suggests that IFN-is being released at ulcer sites, presumably from infiltrating T cells. Down-regulation of AECA target antigens by IFN-has been previously reported in haemolytic uraemic syndrome [21].…”

Etiological Factors of Recurrent Aphthous Stomatitis: A Common Perplexity

“…It has been shown that in patients with aphthous stomatitis there is a heightened lymphocytotoxic effect directed against oral epithelial cells when compared to unaffected controls. [24][25][26] Evidence for this pathogenetic mechanism is also inferred from observations that tissue biopsies of newly erupted aphthous ulcerations demonstrate agglomeration of activated T lymphocytes at the periphery of the lesions, whereas in well-established aphthae the initially predominant CD4…”

“…[22][23][24] From the observations of several investigators it has been hypothesized that the entire process of aphthous ulceration, from initiation through progression, is instigated by the expression on oral epithelial cells of not only normally found HLA class I antigens but also HLA class II antigens. 25 Presumably, this renders the cells antigenically 'foreign' and consequently they become the targets of a cell-mediated immune reaction perpetrated by lymphocytes and Langerhans cells. It has been shown that in patients with aphthous stomatitis there is a heightened lymphocytotoxic effect directed against oral epithelial cells when compared to unaffected controls.…”